Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activation of phosphoinositide-specific phospholipase C by ethanol was compared in hepatocytes isolated from ethanol-fed rats and from pair-fed control animals. Ethanol (100-300 mM) caused a dose-dependent transient increase in cytosolic free Ca2+ levels in indo-1-loaded hepatocytes from both groups of animals. The rate of Ca2+ increase was similar in hepatocytes from control and ethanol-fed rats, but the decay of the Ca2+ increase was somewhat slower in the latter preparation. The ethanol-induced Ca2+ increase caused activation of glycogen phosphorylase, with 50% response at 50 mM-ethanol and a maximal response at 150-200 mM-ethanol, not significantly different in hepatocytes from control and ethanol-fed animals. Ins(1,4,5)P3 formation in response to ethanol (300 mM) or vasopressin (2 nM or 40 nM) was also similar in the two preparations. It is concluded that long-term ethanol feeding does not lead to an adaptive response with respect to the ethanol-induced phospholipase C activation in rat hepatocytes. The ability of ethanol in vitro to decrease membrane molecular order in liver plasma membranes from ethanol-fed and control rats was measured by e.s.r. Membranes from ethanol-fed animals had a significantly lower baseline order parameter compared with control preparations (0.313 and 0.327 respectively), indicative of decreased membrane molecular order. Addition of 100 mM-ethanol significantly decreased the order parameter in control preparations by 2.1%, but had no effect on the order parameter of plasma membranes from ethanol-fed rats, indicating that the plasma membranes had developed tolerance to ethanol, similar to other membranes in the liver. Thus the membrane structural changes associated with this membrane tolerance do not modify the ethanol-induced activation of phospholipase C. The transient activation of phospholipase C by ethanol in hepatocytes may play a role in maintaining an adaptive phenotype in rat liver.
 ...
PMID:Phospholipase C activation by ethanol in rat hepatocytes is unaffected by chronic ethanol feeding. 217 85

Rat hepatocytes were studied for [Ca2+]i with Fura-2 at the single cell level using a microfluorometer-imaging system which showed that both the number of cells elevating [Ca2+]i and the magnitude of [Ca2+]i increase were directly dependent upon ethanol concentration between 50 mM and 1 M. Peak [Ca2+]i increases ranged from 27 nM with 50 mM ethanol to 57 nM after 1 M ethanol. Ethanol appeared to initiate calcium release from intracellular stores and caused a dose dependent production of inositol(1,4,5) triphosphate (Ins(1,4,5)P3) in hepatocytes. Low concentrations of ethanol (50-100 mM) did not significantly raise Ins(1,4,5)P3 although 300 mM-1 M increased Ins(1,4,5)P3 comparable to that found with vasopressin (5 nM). In summary, physiologic amounts of ethanol raise [Ca2+]i in rat hepatocytes, although at lower levels (50-100 mM) the changes may or may not be related to an Ins(1,4,5)P3 pathway.
 ...
PMID:Ethanol-induced increases in [Ca2+]i and inositol (1,4,5) triphosphate in rat hepatocytes. 226 41

Absorption of glycine solution during transurethral resection of the prostate (TURP) changes the serum concentrations of most non-essential amino acids and inhibits diuresis by stimulating release of vasopressin. Ethanol was used as a marker to detect the absorption of irrigant. Measurements of the serum concentrations of vasopressin and amino acids were made in eight patients with absorption volumes from 427 to 1906 ml. Ethanol did not alleviate the vasopressin response to glycine absorption, but changes in the amino acid concentrations in serum became less pronounced than when glycine alone was used.
 ...
PMID:Vasopressin and amino acid concentrations in serum following absorption of irrigating fluid containing glycine and ethanol. 280 91

The effects of hormones on the cytochrome spectra of isolated hepatocytes were recorded under conditions of active gluconeogenesis from L-lactate. Glucagon, phenylephrine, vasopressin and valinomycin, at concentrations that caused stimulation of gluconeogenesis, increased the reduction of the components of the cytochrome bc1 complex, just as has been observed in liver mitochondria isolated from glucagon-treated rats [Halestrap (1982) Biochem. J. 204, 37-47]. The effects of glucagon and phenylephrine were additive. The time courses of the increased reduction of cytochrome c/c1 and NAD(P)H/NAD(P)+ caused by hormones, valinomycin, A23187 and ethanol were measured by dual-beam spectrophotometry and fluorescence respectively. Ethanol (14 mM) produced a substantial rise in NAD(P)H fluorescence, beta-hydroxybutyrate/acetoacetate and lactate/pyruvate ratios, no change in cytochrome c/c1 reduction, a 10% decrease in O2 consumption and a 60% decrease in gluconeogenesis. Glucagon, phenylephrine and vasopressin caused a substantial and transient rise in NAD(P)H fluorescence, but a sustained increase in cytochrome c/c1 reduction and the rates of O2 consumption and gluconeogenesis. The transience of the fluorescence response was greater in the absence of Ca2+, when the cytochrome c/c1 response also became transient. The fluorescence response was smaller and less transient, but the cytochrome c/c1 response was greater, in the presence of fatty acids. Both responses were greatly decreased by the presence of 1 mM-pent-4-enoate. Valinomycin (2.5 nM) caused a decrease in NAD(P)H fluorescence coincident with an increase in cytochrome c/c1 reduction and the rate of gluconeogenesis and O2 consumption. A23187 (7.5 mM) caused increases in both NAD(P)H fluorescence and cytochrome c/c1 reduction. The effects of hormones and valinomycin on the time courses of NAD(P)H fluorescence, cytochrome c/c1 reduction and light-scattering by hepatocytes were compared with those of 0.5 microM-Ca2+ or 1 nM-valinomycin on the same parameters of isolated liver mitochondria. It is concluded that hormones increase respiration by hepatocytes in a biphasic manner. An initial Ca2+-dependent activation of mitochondrial dehydrogenases rapidly increases the mitochondrial [NADH], which is followed by a volume-mediated stimulation of fatty acid oxidation and electron flow between NADH and cytochrome c. 10. Amytal (0.5 mM) was able to reverse the effects of hormones on the reduction of cytochromes c/c1 and the rates of gluconeogenesis and O2 consumption without significantly lowering tissue [ATP].(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:The mechanism of the hormonal activation of respiration in isolated hepatocytes and its importance in the regulation of gluconeogenesis. 302 26

The short-term effects of ethanol on calcium homeostasis were studied in isolated hepatocytes. Ethanol caused a rapid transient activation of phosphorylase not associated with changes in cAMP levels which peaked after 20-30 s and declined slowly over a period of 5-10 min. Maximal activation was found with 200 mM ethanol, and a significant effect was observed at 25 mM ethanol. Similar effects were induced by other organic solvents and by halothane, with more hydrophobic agents being effective at lower concentrations. In hepatocytes loaded with the intracellular calcium indicator quin2, the addition of ethanol caused a transient increase in cytosolic free calcium, with a kinetic pattern compatible with its involvement in the activation of phosphorylase. Pretreatment of the hepatocytes with phenylephrine or vasopressin to deplete the hormone-sensitive calcium pools in the cells prevented the ethanol-induced calcium mobilization. In 32P-labeled hepatocytes addition of ethanol caused a small (5-7%) decrease in the level of [32P]phosphatidylinositol 4,5-bisphosphate and a 10-15% increase in [32P]phosphatidylinositol 4-phosphate and [32P]phosphatidic acid. In hepatocytes labeled with myo-[3H]inositol, ethanol induced a 50-100% increase in the levels of inositol 1,4,5-trisphosphate, inositol 1,3,4-trisphosphate, and inositol bisphosphate. The changes in the inositol 1,4,5-trisphosphate level due to ethanol paralleled the time course of the elevation of cytosolic free calcium levels and activation of phosphorylase a. The effects of ethanol were comparable to those of a physiologic (1 nM) dose of vasopressin; however, unlike with vasopressin, the inositol phosphates and cytosolic calcium levels declined to basal levels 2 min after the addition of ethanol. These results indicate that ethanol, in common with calcium-mobilizing hormones, activates hormone-sensitive phosphoinositide-specific phospholipase C. The resulting changes in inositol 1,4,5-trisphosphate can account for the mobilization of intracellular calcium and the consequent activation of phosphorylase by ethanol.
 ...
PMID:Ethanol-induced mobilization of calcium by activation of phosphoinositide-specific phospholipase C in intact hepatocytes. 302 63

The effects of ethanol administration on activity and regulation of carnitine palmitoyltransferase I (CPT-I) were studied in hepatocytes isolated from rats fed a liquid, high-fat diet containing 36% of total calories as ethanol or an isocaloric amount of sucrose. Cells were isolated at several time points in the course of a 5-week experimental period. Ethanol consumption markedly decreased CPT-I activity and increased enzyme sensitivity to inhibition by exogenously added malonyl-CoA. Changes in enzyme activity occurred sooner than those in enzyme sensitivity. Fatty acid oxidation to CO2 and ketone bodies was depressed in hepatocytes from ethanol-fed animals during the first part of the treatment. At the end of the 35-day period, there were no longer differences in the rate of ketogenesis between the two groups. At that time, however, the rate of CO2 formation was still impaired in the ethanol-fed animals. Furthermore, addition of ethanol or acetaldehyde to the incubation medium strongly depressed CPT-I activity and rates of fatty acid oxidation in hepatocytes from ethanol-treated rats, whereas these effects were much less pronounced in cells from control animals. The response of CPT-I activity to insulin, glucagon, vasopressin, and phorbol ester was blunted in cells derived from ethanol-fed rats. These changes in the regulation of CPT-I activity corresponded with those observed in the rate of fatty acid oxidation. It is concluded that CPT-I may play a role in the generation of the ethanol-induced fatty liver.
 ...
PMID:Effects of ethanol feeding on the activity and regulation of hepatic carnitine palmitoyltransferase I. 306 12

The effect of ethanol on intracellular ionized calcium concentrations (Cai) was studied in synaptosomes isolated from mouse whole brain and in hepatocytes isolated from rat liver. The fluorescent calcium chelator, fura-2, was used to quantitate Cai. Incubation of synaptosomes with ethanol (350-700 mM) increased resting Cai and decreased the effectiveness of KCl to raise Cai in a concentration-dependent manner. Ethanol produced an initial rapid (less than 10 sec) increase in resting Cai that remained elevated for at least 14 min in the presence of the drug. The increase in resting Cai was correlated with the inhibitory effect of ethanol on depolarization-induced increases in Cai. Resting Cai was dependent on the external calcium concentration (0-1 mM). However, the ethanol-induced increase in resting Cai (expressed as percent of control) did not differ in the presence of several extracellular calcium concentrations (0.01, 0.1, and 1 mM). Incubation of synaptosomes in a Na-free buffer resulted in a higher resting Cai and slightly enhanced the effect of ethanol to increase resting Cai. In contrast to these results in brain tissue, ethanol (30-600 mM) did not alter resting Cai or vasopressin-stimulated increases in Cai in hepatocytes. Our results suggest that the anesthetic effects of alcohols may be mediated, in part, by increased resting Cai and by decreased calcium influx through voltage-sensitive calcium channels. In addition, our findings suggest possible mechanisms by which ethanol increases resting Cai in neuronal tissue.
 ...
PMID:Effect of ethanol on intracellular ionized calcium concentrations in synaptosomes and hepatocytes. 369 60

To evaluate the role of antidiuretic hormone (ADH) in the defect in water excretion which is characteristic of glucocorticoid deficiency, the effects of hydrocortisone and ethanol upon urinary dilution during a sustained water load were studied in patients with anterior hypopituitarism. A spectrum of defects in urinary dilution was found in the seven patients with anterior hypopituitarism, and the subjects were separable into two groups. Four patients were unable to excrete a urine hypotonic to plasma (group I) while three diluted the urine (group II). In two of the group II patients, despite maintenance of hydration, urinary osmolality later rose to hypertonicity. Physiological doses of hydrocortisone improved urinary dilution in all patients. Submaximal doses of oral hydrocortisone, when given to the group I patients, converted their response to hydration to one characteristic of the group II patients, i.e., an initial hypotonic urine followed by a secondary rise to hypertonicity. Ethanol, a known inhibitor of ADH secretion, had no effect in the group I patients. When two of these patients were pretreated with sub-maximal doses of hydrocortisone, however, so that they were able to transiently dilute the urine, ethanol prevented the secondary rise in urine osmolality. Similarly, the administration of ethanol to the untreated group II patients, when the urine was hypotonic, improved diluting ability as characterized by a lowering of urinary osmolality and an increased excretion of solute-free water in all three patients. Hydrocortisone did not improve urinary dilution in three patients with complete hypophyseal diabetes insipidus and one with both anterior and posterior insufficiency receiving constant infusions of vasopressin. These data suggest, therefore, that inappropriately elevated levels of ADH play a major role in the defect in water excretion of anterior hypopituitarism. Glucocorticoids appear to be necessary for a normal neurohypophyseal response to inhibitory stimuli.
 ...
PMID:Role of antidiuretic hormone in the abnormal water diuresis of anterior hypopituitarism in man. 509 63

The effects of 75 ml ethanol ingested over 60 min on plasma osmolality (Posmol) and plasma vasopressin (PAVP) in four normal subjects were studied. In the 1st h of the investigation PAVP fell, then rose, even though plasma ethanol levels were still rising. The rise in PAVP was preceded by a rise in Posmol corrected for the influence of ethanol. The fall in PAVP was followed by an increase in free water clearance and a decrease in urine osmolality, while the later rise in PAVP was followed by a decrease in free water clearance (CH2O) and a rise in urine osmolality. The relationship between PAVP and Posmol was then studied during intravenous (iv) hypertonic saline infusion in five subjects. The results were compared with those from a second infusion in the same subjects after ingestion of ethanol (0.5 ml/kg). Ethanol reduced vasopressin release in response to iv hypertonic saline infusion, and this correlated with a reduced decrease in CH2O. We conclude that ethanol inhibits PAVP release by decreasing the response of the osmosodium receptors to changes in plasma tonicity.
 ...
PMID:Effect of ethanol ingestion on plasma vasopressin and water balance in humans. 708 77

Oxytocin administration in rat infused with hypotonic saline is associated with a saliuresis and altered renal water excretion. The role of vasopressin in determining the pattern of oxytocin-induced changes in urine flow was investigated in Long Evans and vasopressin-deficient Brattleboro rats, which exhibit contrasting diuretic and antidiuretic responses to oxytocin. Ethanol anaesthesia and water loading in Long Evans suppressed plasma vasopressin levels and was associated with an antidiuretic response to oxytocin. Vasopressin administration in the Brattleboro rat reversed the oxytocin-induced antidiuresis normally observed in vasopressin deficiency. These results taken with previous observations, have been interpreted as indicative that oxytocin acts as a weak agonist at the renal vasopressin receptor. When plasma vasopressin is suppressed or absent oxytocin acts as a weak antidiuretic agent, but in the presence of higher vasopressin levels a diuretic response to oxytocin is seen which follows displacement of vasopressin, the more potent antidiuretic agent, from the renal receptor.
 ...
PMID:The influence of vasopressin on oxytocin-induced changes in urine flow in the male rat. 711 93


<< Previous 1 2 3 4 Next >>